| First Author | Culshaw S | Year | 2005 |
| Journal | Eur J Immunol | Volume | 35 |
| Issue | 5 | Pages | 1438-44 |
| PubMed ID | 15789357 | Mgi Jnum | J:97796 |
| Mgi Id | MGI:3576421 | Doi | 10.1002/eji.200425661 |
| Citation | Culshaw S, et al. (2005) Prior elevation of IL-18 promotes rapid early IFN-gamma production during staphylococcal infection. Eur J Immunol 35(5):1438-44 |
| abstractText | Systemic Staphylococcus aureus infection is associated with significant morbidity and mortality arising from both bacterial and host immune factors. IL-18 is a pro-inflammatory cytokine of the IL-1 superfamily that exhibits broad functional effects in innate and acquired immune responses and which has been found in high levels in several chronic inflammatory and autoimmune diseases. Over-expression of IL-18 may promote early resolution of infection or could promote a detrimental exaggerated immune response. This was explored in a model of S. aureus infection. We report increased mortality in Swiss mice that were given recombinant IL-18 prior to inoculation with S. aureus LS-1. IL-18 administration prior to infection induced preferentially enhanced IFN-gamma mRNA expression in peripheral blood leukocytes and spleen, especially splenic NK cells. This correlated with increased IFN-gamma protein detection in serum, and leukocyte and spleen cultures at subsequent discrete time points. These data suggest that increased mortality following gram-positive infection in autoimmune diseases could in part reflect the impact of high levels of pleiotropic pro-inflammatory cytokines such as IL-18 present prior to the onset of infection. |
